Training Videos > The dynamic role of central sensitization in myofascial pain syndrome

According to the Integrated Hypothesis, MTrPs are the primary source (cause) of nociception in MPS and result from either an acute or chronic local injury to the muscle, leading to dysfunctional motor endplates and local muscle contracture. However, emerging research suggests that neurogenic mechanisms play a foundational role in the formation of MTrPs and manifestations of MPS in the absence of injury to the muscle. The Neurogenic Hypothesis proposes that the clinical manifestations of MPS are initiated, amplified, and perpetuated by central sensitization (C-Sens), without the need for mechanical injury to the muscle. Instead, MTrPs may form secondary to C-Sens (effect) evoked by persistent nociceptive input from a distinct primary pathologic source (somatic or visceral) in the common neuromeric (segmental) field and/or dysfunction of descending pain modulation. C-Sens evokes neurogenic inflammation (with the antidromic release of neuropeptides) into peripheral tissues thereby increasing local pain & tenderness. Moreover, MPS has a broader impact beyond active MTrPs and has significant associations with mood, health-related quality of life and function. In fact, MPS and MTrPs are a type of spectrum disorder of sensitization that manifests clinically by varying symptoms and signs. Understanding the underlying neuro-inflammatory/ segmental mechanisms in muscle will help clinicians identify potential physiologic mechanisms contributing to the dynamic clinical manifestations of chronic MPS. Targeting pain mechanisms has profound implications for optimizing treatment.